Large Animal Neurology. Joe Mayhew

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СКАЧАТЬ of demyelinated CNS axons can occur under various conditions but is not consistent. Interestingly, remyelination in the superficial areas of the CNS is just as likely to be performed by resident and immigrant peripheral Schwann cells as by oligodendrocytes.

       Microglia

      These fixed histiocytes or tissue macrophages of the CNS respond quickly to any insult that results in necrosis and tissue debris, which they phagocytose. They thus can hypertrophy into macrophages. During proliferation, these histiocytes may form nodules or stars at sites of damage to CNS parenchyma and may also accumulate in perivascular cuffs along with monocytic and polymorphonucleated inflammatory cells. They are involved with removal of dead neurons in the process of neuronophagia. Focal or diffuse microgliosis often remains for years as the last recognizable change following lesions in the CNS.

      With prominent damage to CNS parenchyma, often phagocytic mononuclear cells filled with myelin lipid debris accumulate. These are gitter cells and for the most part are believed to arise from an influx of circulating monocytes, as opposed to proliferation of microglial cells.

       Meningeal, choroidal, and ependymal cells

      These cells tend to be relatively nonreactive. Invasion by infectious agents and direct injury result in an influx of circulating inflammatory and phagocytic cells around them, with some cell proliferation. Subependymal and subpial gliosis can be prominent in some superficial CNS infections. These cells become flattened when CSF pressure is increased within the neuraxis. Fibroblasts associated with the meninges are effective in proliferation and migration, and they cover any meningeal or submeningeal defects that occur with damage.

       Schwann cells

      Proliferated Schwann cells mainly guide and ensheath regrowing axons during the process of Wallerian regeneration in the PNS. Thus, following focal or diffuse PNS axonal lesions, such proliferation is evident. Schwann cells, like oligodendrocytes, are subject to immune and toxic attack and are sometimes affected by inherent metabolic disorders. This may occur before or after normal developmental myelination, causing hypomyelination or demyelination, respectively. Unlike oligodendrocytes, Schwann cells are quite efficient at recoating bare PNS axons and repairing lesions. They do not appear to contribute to the often impressive Renaut body formation in peripheral nerves (Figure 4.6).

Neuropathologic responses in the various mechanisms of disease

      Interpretation of neurohistopathologic sections and reports can be made with consultation of current reference books^2,6 and especially e‐libraries such as the Cornell University Atlas of Veterinary Neuropathology²⁷ and others.^28,29

      Just as each mechanism of disease has its own clinical characteristics as outlined in Chapter 2, so each has certain morphologic characteristics. Thus, one must understand that vascular disorders result in abrupt, localized hypoxia and tissue necrosis, as well as the leakage of blood protein and pigments. This is as clinically relevant as understanding that such diseases usually have a sudden onset of signs that remain static or, more frequently, improve with time: consider fibrocartilaginous emboli in pigs and equine herpesvirus myeloencephalopathy.

       Malformations

      Neurologic signs can result from malformations that involve nervous tissue or involve the tissues surrounding the neuraxis, particularly the cranium and vertebral column. Cranial and vertebral malformations do not always affect the nervous system, but when they do, it is affected by trauma and often signs are progressive. Malformations may be congenital or acquired, and in both cases can have a hereditary, infectious, toxic, traumatic, or even vascular basis. The type of nervous tissue malformation that results often depends more on the time and site of action rather than the causative factors. Thus, certain infections and toxins may result in the same malformation such as cerebellar hypoplasia or arthrogryposis when acting at the appropriate developmental stage.

       Infectious, inflammatory, and immune disorders

      With a few important exceptions, these result in degrees of inflammatory cell infiltrate, at least in the early stages.

      Viruses

Most viral diseases cause nonsuppurative inflammation with lymphocytes, plasma cells, and monocytes, especially accumulating as perivascular cuffs. A few fulminant viral infections, particularly those that result in considerable necrosis of CNS tissue, are characterized by neutrophil invasion. Neurotropic viruses such as rabies and the arboviral encephalitides destroy neurons so there is neuronal degeneration, satellitosis, and neuronophagia. The rarer “slow‐viral” infections such as Maedi/Visna virus infection may not induce much of an inflammatory response and are slowly progressive.

      Bacteria

Suppurative meningitis is most common in neonatal animals, especially those with failure of passive transfer of immunoglobulin. Often there is considerable protein exudate with tissue swelling. When subacute to chronic accumulations of predominantly polymorphonuclear inflammatory cells become sectioned off from CNS parenchyma with astrofibrosis, then a true brain abscess is formed and can act as a space‐occupying lesion causing compression and edema of adjacent tissue. Because of the rigidity of the calvaria, these forms of brain swelling can result in herniation of adjacent parts of the brain (Figures 4.7 and 4.8).³⁰ Vertebral osteomyelitis most often causes spinal cord compression rather than myelitis, and at least initially even septic emboli damage CNS tissue because of ischemic and hemorrhagic infarction.

      Fungi

Fungal infections of the nervous system are rare (Figure 4.9). The usual result is a mixed neutrophilic and mononuclear inflammation, and granulomata may form. Sometimes immunocompromisation is associated with fungal infections.

Figure 4.7 In distinction from caudal herniation of cerebrum and cerebellum with cerebral and brain swelling (Figures 4.8 and 4.10), occasionally a space occupying cerebellar lesion can cause unusual herniation of brain tissue. This is seen here in a dorsal view of the brain from a yearling heifer that suffered from a rostral cerebellar abscess (situated under the arrow) causing rostral herniation of the cerebellar vermis under the tentorium cerebelli. The position of the removed lateral portions of the tentorium cerebelli is depicted by the yellow bars. Ultimately, the midbrain, with the CN‐III oculomotor nerves beneath, will be compressed ventrally by such herniated tissue.

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